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Defibrotide activity in experimental frostbite injury
The pathogenesis of frostbite injury has not been completely elucidated although the available evidence suggests it is an inflammatory reaction following reperfusion injury. Defibrotide given i.p. at 40 mg/kg/day for three days to rabbits, the ears of which were subjected to frostbite, decreased the...
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| Published in: | British journal of plastic surgery 1998-09, Vol.51 (6), p.450-454 |
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| Main Authors: | , , , , , |
| Format: | Article |
| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c368t-e56af3b3d305769f15b6ca3d331f3ff7e316732924ba4fff76d39057c05feb3e3 |
| container_end_page | 454 |
| container_issue | 6 |
| container_start_page | 450 |
| container_title | British journal of plastic surgery |
| container_volume | 51 |
| creator | Özyazgan, rfan Günay, Galip K. Tercan, Mustafa Bekerecilu, Mehmet Melli, Mehmet Üstün, Hüseyin |
| description | The pathogenesis of frostbite injury has not been completely elucidated although the available evidence suggests it is an inflammatory reaction following reperfusion injury. Defibrotide given i.p. at 40 mg/kg/day for three days to rabbits, the ears of which were subjected to frostbite, decreased the presence of inflammatory cells (mast cells −76%; neutrophils −40.4%) and increased prostaglandin I
2 (PGI
2) (as 6-Keto-PGF
1α) in the involved skin. Thromboxane A
2 (TxA
2) (as TxB
2) was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite. |
| doi_str_mv | 10.1054/bjps.1997.0061 |
| format | article |
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2 (PGI
2) (as 6-Keto-PGF
1α) in the involved skin. Thromboxane A
2 (TxA
2) (as TxB
2) was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite.</description><identifier>ISSN: 0007-1226</identifier><identifier>EISSN: 1465-3087</identifier><identifier>DOI: 10.1054/bjps.1997.0061</identifier><identifier>PMID: 9849365</identifier><identifier>CODEN: BJPSAZ</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>6-Ketoprostaglandin F1 alpha - metabolism ; Animals ; Biological and medical sciences ; Female ; Fibrinolytic Agents - therapeutic use ; Frostbite - drug therapy ; Frostbite - metabolism ; Frostbite - pathology ; Injuries of the skin. Diseases of the skin due to physical agents ; Leukocyte Count ; Male ; Mast Cells - pathology ; Medical sciences ; Neutrophils - pathology ; Platelet Aggregation Inhibitors - therapeutic use ; Polydeoxyribonucleotides - therapeutic use ; Rabbits ; Skin - metabolism ; Skin - pathology ; Thromboxane A2 - metabolism ; Traumas. Diseases due to physical agents</subject><ispartof>British journal of plastic surgery, 1998-09, Vol.51 (6), p.450-454</ispartof><rights>1998 The British Association of Plastic Surgeons</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-e56af3b3d305769f15b6ca3d331f3ff7e316732924ba4fff76d39057c05feb3e3</citedby><cites>FETCH-LOGICAL-c368t-e56af3b3d305769f15b6ca3d331f3ff7e316732924ba4fff76d39057c05feb3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2389679$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9849365$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Özyazgan, rfan</creatorcontrib><creatorcontrib>Günay, Galip K.</creatorcontrib><creatorcontrib>Tercan, Mustafa</creatorcontrib><creatorcontrib>Bekerecilu, Mehmet</creatorcontrib><creatorcontrib>Melli, Mehmet</creatorcontrib><creatorcontrib>Üstün, Hüseyin</creatorcontrib><title>Defibrotide activity in experimental frostbite injury</title><title>British journal of plastic surgery</title><addtitle>Br J Plast Surg</addtitle><description>The pathogenesis of frostbite injury has not been completely elucidated although the available evidence suggests it is an inflammatory reaction following reperfusion injury. Defibrotide given i.p. at 40 mg/kg/day for three days to rabbits, the ears of which were subjected to frostbite, decreased the presence of inflammatory cells (mast cells −76%; neutrophils −40.4%) and increased prostaglandin I
2 (PGI
2) (as 6-Keto-PGF
1α) in the involved skin. Thromboxane A
2 (TxA
2) (as TxB
2) was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite.</description><subject>6-Ketoprostaglandin F1 alpha - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Fibrinolytic Agents - therapeutic use</subject><subject>Frostbite - drug therapy</subject><subject>Frostbite - metabolism</subject><subject>Frostbite - pathology</subject><subject>Injuries of the skin. Diseases of the skin due to physical agents</subject><subject>Leukocyte Count</subject><subject>Male</subject><subject>Mast Cells - pathology</subject><subject>Medical sciences</subject><subject>Neutrophils - pathology</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Polydeoxyribonucleotides - therapeutic use</subject><subject>Rabbits</subject><subject>Skin - metabolism</subject><subject>Skin - pathology</subject><subject>Thromboxane A2 - metabolism</subject><subject>Traumas. 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Diseases of the skin due to physical agents</topic><topic>Leukocyte Count</topic><topic>Male</topic><topic>Mast Cells - pathology</topic><topic>Medical sciences</topic><topic>Neutrophils - pathology</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Polydeoxyribonucleotides - therapeutic use</topic><topic>Rabbits</topic><topic>Skin - metabolism</topic><topic>Skin - pathology</topic><topic>Thromboxane A2 - metabolism</topic><topic>Traumas. 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Defibrotide given i.p. at 40 mg/kg/day for three days to rabbits, the ears of which were subjected to frostbite, decreased the presence of inflammatory cells (mast cells −76%; neutrophils −40.4%) and increased prostaglandin I
2 (PGI
2) (as 6-Keto-PGF
1α) in the involved skin. Thromboxane A
2 (TxA
2) (as TxB
2) was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>9849365</pmid><doi>10.1054/bjps.1997.0061</doi><tpages>5</tpages></addata></record> |
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| identifier | ISSN: 0007-1226 |
| ispartof | British journal of plastic surgery, 1998-09, Vol.51 (6), p.450-454 |
| issn | 0007-1226 1465-3087 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70128201 |
| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | 6-Ketoprostaglandin F1 alpha - metabolism Animals Biological and medical sciences Female Fibrinolytic Agents - therapeutic use Frostbite - drug therapy Frostbite - metabolism Frostbite - pathology Injuries of the skin. Diseases of the skin due to physical agents Leukocyte Count Male Mast Cells - pathology Medical sciences Neutrophils - pathology Platelet Aggregation Inhibitors - therapeutic use Polydeoxyribonucleotides - therapeutic use Rabbits Skin - metabolism Skin - pathology Thromboxane A2 - metabolism Traumas. Diseases due to physical agents |
| title | Defibrotide activity in experimental frostbite injury |
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